Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2

被引：1275

作者：

Aliprantis, AO

Yang, RB

Mark, MR

Suggett, S

Devaux, B

Radolf, JD

Klimpel, GR

Godowski, P

Zychlinsky, A

机构：

[1] NYU, Sch Med, Skirball Inst, New York, NY 10016 USA

[2] NYU, Sch Med, Dept Microbiol, New York, NY 10016 USA

[3] Genentech Inc, Antibody Technol Grp, S San Francisco, CA 94080 USA

[4] Genentech Inc, Dept Mol Biol, S San Francisco, CA 94080 USA

[5] Univ Connecticut, Ctr Hlth, Ctr Microbial Pathogenesis, Farmington, CT 06030 USA

[6] Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA

来源：

SCIENCE | 1999年 / 285卷 / 5428期

关键词：

D O I：

10.1126/science.285.5428.736

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 [理学]; 0710 [生物学]; 09 [农学];

摘要：

Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappa B, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.

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收藏

页码：736 / 739

页数：4

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